UNASSIGNED: To study associations between fractional exhaled nitric oxide (FeNO) and asthma, airway symptoms, sensitization to common allergens, outdoor pollution and home environment among 380 students in eight junior high schools in two areas in Indonesia.
UNASSIGNED: Data on health and home were collected by a face-to face interview before measuring FeNO and performing skin prick test against common allergens. Exploratory linear mixed and logistic regression models were employed.
UNASSIGNED: Geometric mean of FeNO was 17.8 ppb (GSD 2.09) and 139 students (36.6%) had elevated FeNO (>20 ppb). In total, 107 students (28.2%) were sensitized to house dust mite (HDM) (Der p1 or Der f1), 4 (1.1%) to cat and 3 (0.8%) to mold (Cladosporium or Alternaria). Moreover, 20 students (5.3%) had diagnosed asthma, 38 (10.0%) had current wheeze, and 107 (28.2%) had current rhinitis. HDM sensitization, diagnosed asthma, current wheeze, and current rhinitis were associated with FeNO. In total, 281 students (73.9%) had mold or dampness, 232 (61.1%) had environmental tobacco smoke (ETS) and 43 (11.3%) had other odor at home. Indoor mold or dampness and other odor at home were associated with FeNO. ETS was negatively associated with FeNO.
UNASSIGNED: HDM sensitization and elevated FeNO can be common among children in this part of Indonesia. The high prevalence of elevated FeNO indicate that undiagnosed childhood asthma is common. Dampness, mold and odor at home can be associated with increased FeNO while ETS can be associated with decreased FeNO.

The detrimental effects of environmental tobacco smoke (ETS) on women\'s reproductive health have been widely recognized. However, the detailed association between exposure to environmental tobacco smoke and the incidence of infertility remains under-explored. This investigation focuses on exploring this potential connection.
For this analysis, we extracted data from the US National Health and Nutrition Examination Survey (NHANES) database, covering the years 2013 to 2018, focusing on individuals with recorded serum cotinine levels and infertility information. ETS exposure and fertility status were analyzed as independent and dependent variables, respectively. We applied weighted multivariate logistic regression method to evaluate the impact of ETS on infertility, including subgroup analyses for more detailed insights.
The study encompassed 3,343 participants. Logistic regression analysis revealed a notable positive correlation between ETS exposure and infertility, with an odds ratio (OR) of 1.64 (95% Confidence Interval [CI]: 1.14-2.36). We observed a non-linear relationship between ETS exposure and infertility risk. Notably, infertility risk increased by 64% in serum cotinine levels above 0.136 compared to that in serum cotinine levels below 0.011. Further, subgroup analysis and interaction tests showed consistent results across different segments, underscoring the robustness of the ETS-infertility link.
Our findings suggest that environmental tobacco smoke exposure may be a contributing factor to infertility. These results reinforce the recommendation for women in their reproductive years to avoid ETS exposure, especially when planning for pregnancy.

Environmental tobacco smoke (ETS) is known to cause lung inflammatory and injurious responses. Smoke exposure is associated with the pathobiology related to lung fibrosis, whereas the mechanism that ETS exposure augments pulmonary fibrogenesis is unclear. We hypothesized that ETS exposure could exacerbate fibrotic responses via collagen dynamic dysregulation and complement activation. C57BL/6J and p16-3MR mice were exposed to ETS followed by bleomycin administration. ETS exposure exacerbated bleomycin-induced collagen and lysyl oxidase overexpression in the fibrotic lesion. ETS exposure also led to augmented bleomycin-induced upregulation of C3 and C3AR, which are pro-fibrotic markers. Moreover, overexpressed collagens and C3 levels were highly significant in males than females. The old mice (17 months old) were exposed to ETS and treated with bleomycin to induce fibrogenesis which is considered as an aging-associated disease. Fewer gene and protein dysregulations trends were identified between ETS exposure with the bleomycin group and the bleomycin alone group in old mice. Based on our findings, we suggested that ETS exposure increases the risk of developing severe lung fibrotic responses via collagen overexpression and lysyl oxidase-mediated collagen stabilization in the fibrotic lesion, and potentially affected the complement system activation induced by bleomycin. Further, male mice were more susceptible than females during fibrogenesis exacerbation. Thus ETS and bleomycin induced lung fibrotic changes via collagen-lysyl oxidase in an age-dependent mechanism.

Indoor pollution and deposition dust (DD), in particular, are acquiring concern, due to long exposure time and importance of intake by humans through contact and ingestion. Hospitals look a special category of sites, owing to peculiar contaminants affecting them and to presence of people prone to adverse effects induced by toxicants. Four in-field campaigns aimed at understanding the chemical composition of DD were performed in five Italian hospitals. Measurements were performed before (autumn 2019), during (spring 2021), and after (winter 2022) the peak of SARS-CoV2 and when restrictions caused by pandemic were revoked (winter 2023). Parallel measurements were made outdoors (2022), as well as in a university and a dwelling. Targeted contaminants were n-alkanes and polycyclic aromatic hydrocarbons (PAHs), while iso- and anteiso-alkanes were analyzed to assess the impact of tobacco smoking. Total n-alkanes ranged from 3.9 ± 2.3 to 20.5 ± 4.2 mg/g, with higher percentages of short chain homologs in 2019. PAHs ranged from 0.24 ± 0.22 to 0.83 ± 0.50 mg/g, with light congeners (≤ 228 a.m.u.) always exceeding the heavy ones (≥ 252 a.m.u.). According to carbon preference indexes, alkanes originated overall from anthropogenic sources. Microorganisms resulted to affect a hospital, and tobacco smoke accounted for ~ 4-20‰ of DD mass. As for PAH sources, the diagnostic concentration ratios suggested the concourse of biological matter burning and vehicle emission. Benzo[a]pyrene equivalent carcinogenic and mutagenic potencies of depositions at hospitals ranged ~ 9-39 μg/g and ~ 15-76 μg/g, respectively, which seems of concern for health. DD composition in hospitals was different from that outside the premises, as well as that found at university and at dwelling.

Few population studies have sufficient follow-up period to examine early-life exposures with later life diseases. A critical question is whether involuntary exposure to tobacco smoke from conception to adulthood increases the risk of cardiometabolic diseases (CMD) in midlife. In the Collaborative Perinatal Project, serum-validated maternal smoking during pregnancy (MSP) was assessed in the 1960s. At a mean age of 39 years, 1623 offspring were followed-up for the age at first physician-diagnoses of any CMDs, including diabetes, heart disease, hypertension, or hyperlipidemia. Detailed information on their exposure to environmental tobacco smoke (ETS) in childhood and adolescence was collected with a validated questionnaire. Cox regression was used to examine associations of in utero exposure to MSP and exposure to ETS from birth to 18 years with lifetime incidence of CMD, adjusting for potential confounders. We calculated midlife cumulative incidences of hyperlipidemia (25.2%), hypertension (14.9%), diabetes (3.9%), and heart disease (1.5%). Lifetime risk of hypertension increased by the 2nd -trimester exposure to MSP (adjusted hazard ratio: 1.29, 95% confidence interval: 1.01-1.65), ETS in childhood (1.11, 0.99-1.23) and adolescence (1.22, 1.04-1.44). Lifetime risk of diabetes increased by joint exposures to MSP and ETS in childhood (1.23, 1.01-1.50) or adolescence (1.47, 1.02-2.10). These associations were stronger in males than females, in never-daily smokers than lifetime ever smokers. In conclusion, early-life involuntary exposure to tobacco smoke increases midlife risk of hypertension and diabetes in midlife.

Depression is associated with both environmental tobacco smoke (ETS) and inflammation. However, whether systemic inflammation mediates the ETS-depression relationship is unclear.
We analyzed 19,612 participants from the 2009-2018 National Health and Nutrition Examination Survey (representing approximately 206,284,711 USA individuals), utilizing data of depressive symptoms (assessed by Patient Health Questionnaire-9), blood cotinine level (an ETS biomarker), dietary inflammatory index (DII, assessed by 24-h dietary recall) and inflammation, represented by immune-inflammation index (SII) and systemic inflammation response index (SIRI).
Weighted multivariable logistic regression showed that a higher blood cotinine level is significantly associated with a higher depressive symptoms risk (OR = 1.79, 1.35-2.38). After adjusting for covariates, the effect in smokers (OR = 1.220, 95 % CI: 1.140-1.309) is larger than that in non-smokers (OR = 1.150, 95 % CI: 1.009-1.318). Compared to the lowest level, depressive symptoms risks in participants with the highest level of SII, SIRI and DII are 19 % (OR = 1.19, 1.05-1.35), 15 % (OR = 1.15, 1.01-1.31) and 88 % (OR = 1.88, 1.48-2.39) higher, respectively. Weighted linear regression demonstrated positive correlations of SII (β = 0.004, 0.001-0.006), SIRI (β = 0.009, 0.005-0.012) and DII (β = 0.213, 0.187-0.240) with blood cotinine level. Restricted cubic splines model showed a linear dose-response relationship between blood cotinine and depressive symptoms (Pnon-linear = 0.410), with decreasing risk for lower DII. And SII and SIRI respectively mediate 0.21 % and 0.1 % of the association between blood cotinine and depressive symptoms.
Cross-sectional design, and lack of medication data for depression.
Positive association of ETS (blood cotinine) with depressive symptoms risk is partly mediated by systemic inflammation, and anti-inflammatory diet could be beneficial.

BACKGROUND: Environmental tobacco smoke (ETS) exposure in children can cause delayed lung development and lifelong cardiovascular damage. The aim of this study was to measure ETS exposure in children in Israel in 2020-2021 using urinary cotinine (UC) measurements and to assess correlates of ETS exposure, including parental smoking.
METHODS: In the framework of the National Human Biomonitoring Program, spot urine samples and questionnaire data were collected from 166 children aged 4-12 years, during the years 2020-2021. We collected urine samples in 233 adults, 69 of whom were parents of children included in the study. Parents of participating children were asked about parental smoking, child\'s exposure to ETS and smoking policy at home. Cotinine and creatinine were measured in urine. Creatinine-adjusted and unadjusted urine cotinine (UC) geometric means were calculated. Associations between potential correlates and UC concentrations were analyzed in univariate and multivariate analyses. For 69 child-parent pairs, correlation between child and parental UC was analyzed.
RESULTS: Based on urinary cotinine measurement, 65.2% of children of smokers are exposed to ETS, compared to 20.7% of children in non-smoking families. Greater numbers of smokers living in the home (beta = 1.27, p < 0.01), and low maternal education (beta = - 2.32, p < 0.01) were associated with higher levels of UC in a multivariate analysis. Spearman correlations showed a positive moderate correlation between UC in 69 child-parent pairs (r = 0.52, p < 0.01).
CONCLUSIONS: In order to reduce child exposure to ETS, smoking parents should be urgently targeted for smoking cessation and smoke-free home interventions. Further interventions are needed to protect all children from ETS.

Canine urothelial carcinoma (UC) initially responds favorably to treatment, but is ultimately lethal in most cases. Research to identify modifiable risk factors to prevent the cancer is essential. The high breed-associated risk for UC, e.g. 20-fold higher in Scottish terriers, can facilitate this research. The objective was to identify environmental and host factors associated with UC in a cohort of Scottish terriers. Information was obtained through dog owner questionnaires for 120 Scottish terriers ≥ 6 years old participating in a bladder cancer screening study, with comparisons made between dogs that did or did not develop UC during the 3 years of screening. Univariable models were constructed, and variables with P < 0.20 were included when building the multivariable model, and then removed using a backward stepwise procedure. P < 0.05 was considered statistically significant. Urine cotinine concentrations were measured by liquid chromatography-mass spectrometry to further investigate potential cigarette smoke exposure. Biopsy-confirmed UC which was found in 32 of 120 dogs, was significantly associated with the dogs living in a household with cigarette smokers (odds ratio [OR], 6.34; 95 % confidence intervals [CI], 1.16-34.69; P = 0.033), living within a mile of a marsh or wetland (OR, 21.23; 95 % CI, 3.64-123.69; P = 0.001), and history of previous bladder infections (OR, 3.87; 95 % CI, 1.0-14.98; P = 0.050). UC was diagnosed in 18 of 51 dogs (35.3 %) with quantifiable cotinine concentrations, and six of 40 dogs (15.0 %) without quantifiable cotinine concentrations in their urine (P = 0.0165). In conclusion, the main modifiable risk factor for UC in this cohort of dogs was exposure to second-hand tobacco smoke.

Exposure to environmental tobacco smoke (ETS) is arguably the most ubiquitous and hazardous, even at very low levels, starting in early life. The objective of this study was to describe the state of research and future trends on ETS exposure and Children\'s Health (CH) topics with bibliometrics and altmetrics.
An electronic search was performed in Scopus database on January 31, 2023. Consensus was arrived on 100 most-cited articles by two reviewers. These papers were then cross matched with citations harvested from Web of Science (WoS) and Google Scholar. Altmetric Attention Score (AAS) and Dimension counts were also collected. Analysis and network visualization of authors, countries, and keywords were generated using VOSviewer software.
Among a total of 1107 articles published on ETS and CH, the 100 top-cited articles appeared in 54 journals, with Pediatrics (n = 12) contributing a maximum number of articles. The time period between 2000 and 2009 accounted for 44% of all publications. With respect to the research design employed across these studies, cross-sectional design took precedence over others accounting for approximately 40%. Predominantly, articles focused on childhood asthma; however, current research trends have shifted towards emerging fields such as children\'s oral health and DNA methylation. Twitter, policy documents, and news outlets were the main platforms where outputs were discussed. The AAS was not associated with journal impact factor or access type. Weak correlations were observed between AAS and citation count in Scopus, WoS, and Google Scholar (r = 0.17 to 0.27) while a positive association existed between dimension count and the number of citations across all three databases (r = 0.84 to 0.98).
This study demonstrates the evolution, digital dissemination and research hotspots in the field of ETS and CH, predicting the possible future research directions. High-quality studies with more specific exposure classification are warranted to better understand the relationship between ETS and CH.

Environmental tobacco smoke (ETS) exposure has been proven to induce digestive diseases such as hepatic steatosis, cirrhosis, and gastrointestinal cancer, yet little is known about the link between ETS exposure and constipation. This study aimed to investigate the impact of ETS exposure on the risk of chronic constipation in adults aged 20 years or older. This is a cross-sectional study based on population. A total number of 7705 participants from the National Health and Nutrition Examination Survey (NHANES) 2005-2010 were included. Cotinine, an alkaloid found in tobacco, serves as a reliable and precise biomarker for measuring exposure to ETS. Hence, the categorization of exposure to ETS was conducted based on serum cotinine levels, resulting in four distinct categories. The association between ETS exposure and the risk of constipation was assessed using multivariable restricted cubic spline and logistic regression with odds ratio (OR) and 95% confidence interval (CI). The weighted prevalence of constipation in this study was estimated to be 7.51% based on stool consistency, or 3.11% based on stool frequency. The fully adjusted models indicated a positive correlation between exposure to ETS and constipation as measured by stool frequency, among adults with poor dietary quality (OR (95% CI): moderate exposure: 2.49 (1.05, 5.94); high exposure: 2.36(1.13, 4.95), P for trend = 0.03), while no significant difference was observed in the subgroup with a higher healthy eating index. Furthermore, the log10-transformed serum cotinine level exhibited a non-linear inverted U-shaped association with constipation in individuals with poor dietary quality (P overall = 0.0207, P non-linear = 0.0427). Conversely, a J-shaped non-linear relationship was observed in the subgroup with a higher healthy eating index (P overall = 0.0028, P non-linear = 0.0036). Our results show that ETS exposure appears to be positively associated with stool frequency-related chronic constipation in adults with poor dietary quality.